LVH Plus Myocardial Injury Flags HF Risk in Black Patients

Marlene Busko

December 28, 2018

African Americans with the combination of myocardial injury, identified by high levels of high-sensitivity cardiac troponin I (hs-cTnI) and left ventricular hypertrophy (LVH) on electrocardiogram have a "malignant" preclinical heart failure phenotype that puts them at much higher risk of heart failure than their peers, with the risk especially high in men, new research shows.

Among more than 3000 African Americans without prior cardiovascular disease (CVD) in the Jackson Heart Study, men with both LVH and myocardial injury had a 15-fold increased risk of HF in the next decade compared to those without these two risk factors.

Women with both traits had a four-fold increased risk of this outcome compared to those without them, in the study published online December 19 in JAMA Cardiology.

"High levels of hs-troponin and LVH identify a higher risk phenotype of African Americans, but we need more studies to validate this," lead author Ambarish Pandy, MD, MSCS, University of Texas Southwestern Medical Center, Dallas, cautioned in an interview with | Medscape Cardiology. 

More research is also needed to understand the biology behind the gender difference, to investigate how these measures predict HF risk in other racial/ethnic groups, and to see if the risk can be mitigated by using aggressive strategies to modify other CVD risk factors, he said.

"For now," Pandey said, "if I see a patient who has elevated hs-troponin or LVH on EKG or echo, I would pursue more aggressive risk factor modification with better blood pressure control, more aggressive diabetes control if they have that, weight loss, and encourage exercise or physical activity to meet...or even go beyond the guideline-recommended levels of 30 to 60 minutes of walking per day."

Two Potential Predictors of HF in African Americans

Heart failure affects African Americans, especially those younger than 50 years, more than other races, which may be related to a higher incidence and worse control of hypertension and diabetes, Pandey and colleagues note.

Two markers, subclinical myocardial injury (which can now be readily detected using an hs-cTnI assay) and LVH, have been associated with an increased risk of HF, but this has not been well studied in blacks.  

To investigate this, the researchers identified 3987 African Americans living in the Jackson, Mississippi area who were 21 to 84 years old and free of CVD or HF when they enrolled in the Jackson Heart Study.  

At baseline, an assay was used to determine hs-cTnI levels and an electrocardiogram was used to detect LVH.

Subclinical myocardial injury was defined as hs-cTnI ≥ 4 ng/L in women and ≥ 6 ng/L in men.

Participants were divided into 4 groups:

  • No LVH and no subclinical myocardial injury

  • Subclinical myocardial injury but no LVH

  • LVH but no subclinical myocardial injury

  • LVH and subclinical myocardial injury

A quarter of participants (25%) had subclinical myocardial injury, 6% had LVH, and 3.7% had both.

Compared with participants without subclinical myocardial injury, those with this risk factor were older (mean age, 61 vs 52 years), more likely to have diabetes (30% vs 17%) and hypertension (77% vs 47%), and had a slightly higher mean body mass index (31 vs 30 kg/m2).

Men with LVH and subclinical myocardial injury had a much higher risk of HF during follow-up (adjusted hazard ratio [aHR], 14.62; 95% CI, 7.61 - 28.10; P < .001) compared with men without either risk factor, after adjusting for age, body mass index, hypertension, diabetes status, HbA1c, systolic blood pressure, current smoking, estimated glomerular filtration rate, and physical activity.

Women with this phenotype had a smaller increased risk of HF (aHR, 3.81; 95% CI, 2.40 - 6.85; P < .001) compared to those without either risk factor.

Having LVH without myocardial injury "may not be as bad," Pandey noted.

Among those without myocardial injury, men with LVH had a 3.83-fold increased risk of HF (P = .016) and women with LVH had a nonsignificant 1.14-fold increased risk of HF (P = .78) compared to those without LVH.

Overall, the 3.7% of participants with both LVH and subclinical myocardial injury had a 35% risk of HF within 10 years of follow-up, which is "remarkable," the authors highlight, "considering the relatively young age of the study population (median age, 54 years) and lack of CVD at baseline."

If subsequent research confirms and validates these findings, and if other studies show that screening could lead to better outcomes, combined screening with an hs-cTnI assay and LVH detection would be feasible, Pandey noted.

"Prior studies," the researchers write, "have demonstrated that electrocardiogram-based LVH can substitute for imaging-based LVH, which would make such a screening strategy more cost-effective and readily available."

And "the day is not far when we actually do a randomized controlled trial of [an hs-cTnI] screening strategy to modify risk," Pandey speculates.

The study was funded by the Strategically Focused Research Network Grant for Prevention from the American Heart Association to the University of Texas Southwestern Medical Center, Dallas, and Northwestern University School of Medicine, Chicago. Senior author Jarrett D. Berry received a grant from the American Heart Association prevention network and salary support from Abbott Diagnostics. Funding for biomarker assays was provided by Abbott Diagnostics. Pandey has disclosed no relevant financial relationships. Disclosures of the other authors are listed with the article.

JAMA Cardiology. Published December 19, 2018. Abstract

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